Infant mortality has declined in the United States because of
advances in public health and clinical medicine. Birth defects are
the leading cause of infant mortality (1), but infant
mortality attributable to birth defects (IMBD) has not declined as
rapidly as overall infant mortality. From 1968 to 1995, the
proportion of IMBD increased from 14.5% to 22.2% (2,3). To help
focus efforts to reduce IMBD, CDC examined trends in IMBD,
highlighting demographic, geographic, and defect-specific mortality
rates. This report summarizes the results of this analysis, which
indicate variation in rates for IMBD by sex, race/ethnicity, and
state of residence.

The underlying cause-of-death for all infants (children aged
less than 1 year) was obtained from U.S. public-use, multiple-cause
mortality data tapes maintained by CDC. Birth defects in this study
were classified according to the International Classification of
Diseases, Clinical Modification, Ninth Revision, codes 740-759. The
number of live births per year by the child's race and sex and
mother's state of residence (including the District of Columbia)
was determined from published natality statistics. The number of
live births was 3,612,258 in 1980 and 3,899,589 in 1995 (3). Only
births and deaths to U.S. residents were included in the analyses.

During 1980-1995, IMBD declined 34.2%, and overall infant
mortality declined 39.8% (Table_1). The proportion of overall
infant mortality caused by birth defects increased from 20% to 22%.
Among females, the decrease in IMBD was greater and the rate of
IMBD was lower than among males. Among whites and Asians/Pacific
Islanders, the decreases in IMBD were greater than those among
blacks and American Indians/ Alaskan Natives. As a result, by 1995,
the gap between IMBD in whites and in both blacks and American
Indians/Alaskan Natives increased.

The decline in IMBD varied by organ system (Table_2).
Deaths
associated with defects of the cardiovascular, central nervous,
musculoskeletal, genitourinary, and digestive systems declined
substantially. Deaths associated with trisomies 13 and 18,
reduction defects of the brain, and defects of the respiratory
system increased.

From 1980 to 1995, IMBD declined in every state and the
District of Columbia; however, IMBD was consistently higher in the
South and parts of the Midwest than in other regions
(Figure_1).
This geographic variation persisted when the analysis was
restricted by race. Hawaii, Maryland, Oregon, and Vermont had the
greatest decline in IMBD, moving from the highest category (2.7-3.2
per 1000 live-born infants) to the lowest (1.1-1.4).

Editorial Note

Editorial Note: The findings in this report document a large
decline in IMBD but substantial variations in IMBD across
populations and geographic areas. Efforts to reduce IMBD should
focus on identifying reasons for these variations. The causes of
most birth defects are unknown, and the causes of deaths from birth
defects require further study.

Cardiovascular defects are the single largest contributor to
IMBD. The largest specific cause of cardiovascular IMBD was
hypoplastic left heart syndrome, the rate of which declined
slightly during 1980-1995. Other important causes of cardiovascular
IMBD (e.g., transposition of the great vessels and ventricular
septal defect) declined substantially, probably because of
improvements in treatment.

The second largest contributor to IMBD was central nervous
system defects. The birth prevalence of these defects is affected
by primary prevention (e.g., increased intake of folic acid
initiated before conception), changes in prenatal diagnosis
patterns, and the availability and use of pregnancy termination
services following a prenatal diagnosis of a serious defect. These
factors probably account for some of the decline in anencephalus
and hydrocephalus. IMBD attributable to reduction defects of the
brain has increased dramatically, most likely because of increasing
use of sophisticated imaging techniques that make diagnosis of this
defect more common.

The increase in IMBD attributable to chromosomal defects
includes increases in both trisomies 13 and 18 and a decrease in
trisomy 21. Increases in rates of trisomy 13 and 18 are probably a
result of increased use of diagnostic karyotyping. In comparison,
the decline in deaths attributed to trisomy 21 (Down syndrome) is
probably related to improved treatment for the congenital heart
defects that are the leading cause of deaths among these infants,
and increased use of prenatal diagnosis. The increase in IMBD
attributable to respiratory defects may be associated with an
increasing use of the diagnostic code for lung
agenesis/hypoplasia/dysplasia.

IMBD attributable to musculoskeletal and digestive system
defects has declined dramatically, most likely because of advances
in surgical treatments. In one children's hospital, survival rates
for infants with congenital diaphragmatic hernia improved from 42%
during 1970-1983 to 79% during 1989-1997 (4). In Japan, esophageal
atresia survival increased from an estimated 28% in the late 1950s
and early 1960s to 80% since 1980 (5).

Previous studies have documented substantial racial
differences in the incidence of birth defects and IMBD (6,7),
although the magnitude of these differences vary by the method of
assigning the child's race (8). Higher IMBD in some racial/ethnic
populations may reflect reduced access to perinatal and other
health care associated with disadvantaged socioeconomic status and
other factors that may affect mortality trends. Males consistently
have higher rates of IMBD than females, probably because of the
higher incidence of many birth defects among males (9).

Poverty and access to health care also may affect geographic
variations in IMBD. During 1995, 10 of the 12 states (83%) with
IMBD greater than or equal to 1.9 per 1000 live-born infants were
above the U.S. median for percent of population in poverty (10). In
comparison, only six states would have been above the median if
there was no relation between poverty and IMBD.

The findings in this report are subject to at least two
limitations. First, the reliability of data on IMBD is limited by
the accuracy of demographic and cause-of-death data included on
infant death certificates. In addition, changes in administrative
and diagnostic practices also may affect the validity of the data.

The correlation between poverty and high IMBD suggests that
access to health-care services also may be an important factor
limiting declines in IMBD. Unlike the effect of race and sex, the
effect of poverty on IMBD can be changed. Improving access to
perinatal and other preventive and health-care services is a key
factor in reducing IMBD and overall infant mortality.

Petrini J, Damus K, Roy S, Johnson K, Johnston RB. The effect
of
using "race of child" instead of "race of mother" on the
black-white gap in infant mortality due to birth defects.
Public
Health Rep 1998;113:263-7.

Hay S. Sex differences in the incidence of certain congenital
malformations: a review of the literature and some new data.
Teratology 1971;4:277-86.

Lamison-White L. Current population reports: poverty in the
United
States, 1996. Washington, DC: US Department of Commerce,
Economics
and Statistics Administration, Bureau of the Census, 1997;
series
no. P60-1980.

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